Investigation of mechanisms governing emission of odorants

The literature identifies several models that describe inter-phase mass transfer, key to the emission process. While the emission process is complex and these models may be more or less successful at predicting mass transfer rates, they identify three key variables for a system involving a liquid and an air phase in contact with it: • A concentration (or partial pressure) gradient driving force; • The fluid dynamic characteristics within the liquid and air phases, and • The chemical properties of the individual components within the system. In three applied research projects conducted prior to this study, samples collected with two well-known sampling devices resulted in very different odour emission rates. It was not possible to adequately explain the differences observed. It appeared likely, however, that the sample collection device might have artefact effects on the emission of odorants, i.e. the sampling device appeared to have altered the mass transfer process. This raised the obvious question: Where two different emission rates are reported for a single source (differing only in the selection of sampling device), and a credible explanation for the difference in emission rate cannot be provided, which emission rate is correct? This research project aimed to identify the factors that determine odour emission rates, the impact that the characteristics of a sampling device may exert on the key mass transfer variables, and ultimately, the impact of the sampling device on the emission rate itself. To meet these objectives, a series of targeted reviews, and laboratory and field investigations, were conducted. Two widely-used, representative devices were chosen to investigate the influence of various parameters on the emission process. These investigations provided insight into the odour emission process generally, and the influence of the sampling device specifically.

Mechanisms of change in negative thinking and urinary monoamines in depressed patients during acute treatment with group cognitive behavior therapy and antidepressant medication

This naturalistic study investigated the mechanisms of change in measures of negative thinking and in 24-h urinary metabolites of noradrenaline (norepinephrine), dopamine and serotonin in a sample of 43 depressed hospital patients attending an eight-session group cognitive behavior therapy program. Most participants (91%) were taking antidepressant medication throughout the therapy period according to their treating Psychiatrists' prescriptions. The sample was divided into outcome categories (19 Responders and 24 Non-responders) on the basis of a clinically reliable change index [Jacobson, N.S., & Truax, P., 1991. Clinical significance: a statistical approach to defining meaningful change in psychotherapy research. Journal of Consulting and Clinical Psychology, 59, 12–19.] applied to the Beck Depression Inventory scores at the end of the therapy. Results of repeated measures analysis of variance [ANOVA] analyses of variance indicated that all measures of negative thinking improved significantly during therapy, and significantly more so in the Responders as expected. The treatment had a significant impact on urinary adrenaline and metadrenaline excretion however, these changes occurred in both Responders and Non-responders. Acute treatment did not significantly influence the six other monoamine metabolites. In summary, changes in urinary monoamine levels during combined treatment for depression were not associated with self-reported changes in mood symptoms.

Effects of lead exposure on hippocampal metabotropic glutamate receptor subtype 3 and 7 in developmental rats

Background A complete explanation of the mechanisms by which Pb2+ exerts toxic effects on developmental central nervous system remains unknown. Glutamate is critical to the developing brain through various subtypes of ionotropic or metabotropic glutamate receptors (mGluRs). Ionotropic N-methyl-D-aspartate receptors have been considered as a principal target in lead-induced neurotoxicity. The relationship between mGluR3/mGluR7 and synaptic plasticity had been verified by many recent studies. The present study aimed to examine the role of mGluR3/mGluR7 in lead-induced neurotoxicity. Methods Twenty-four adult and female rats were randomly selected and placed on control or 0.2% lead acetate during gestation and lactation. Blood lead and hippocampal lead levels of pups were analyzed at weaning to evaluate the actual lead content at the end of the exposure. Impairments of short -term memory and long-term memory of pups were assessed by tests using Morris water maze and by detection of hippocampal ultrastructural alterations on electron microscopy. The impact of lead exposure on mGluR3 and mGluR7 mRNA expression in hippocampal tissue of pups were investigated by quantitative real-time polymerase chain reaction and its potential role in lead neurotoxicity were discussed. Results Lead levels of blood and hippocampi in the lead-exposed rats were significantly higher than those in the controls (P < 0.001). In tests using Morris Water Maze, the overall decrease in goal latency and swimming distance was taken to indicate that controls had shorter latencies and distance than lead-exposed rats (P = 0.001 and P < 0.001 by repeated-measures analysis of variance). On transmission electron microscopy neuronal ultrastructural alterations were observed and the results of real-time polymerase chain reaction showed that exposure to 0.2% lead acetate did not substantially change gene expression of mGluR3 and mGluR7 mRNA compared with controls. Conclusion Exposure to lead before and after birth can damage short-term and long-term memory ability of young rats and hippocampal ultrastructure. However, the current study does not provide evidence that the expression of rat hippocampal mGluR3 and mGluR7 can be altered by systemic administration of lead during gestation and lactation, which are informative for the field of lead-induced developmental neurotoxicity noting that it seems not to be worthwhile to include mGluR3 and mGluR7 in future studies. Background

Improved correlation-based modal strain energy method for global damage detection of truss bridge structures

The previous investigations have shown that the modal strain energy correlation method, MSEC, could successfully identify the damage of truss bridge structures. However, it has to incorporate the sensitivity matrix to estimate damage and is not reliable in certain damage detection cases. This paper presents an improved MSEC method where the prediction of modal strain energy change vector is differently obtained by running the eigensolutions on-line in optimisation iterations. The particular trail damage treatment group maximising the fitness function close to unity is identified as the detected damage location. This improvement is then compared with the original MSEC method along with other typical correlation-based methods on the finite element model of a simple truss bridge. The contributions to damage detection accuracy of each considered mode is also weighed and discussed. The iterative searching process is operated by using genetic algorithm. The results demonstrate that the improved MSEC method suffices the demand in detecting the damage of truss bridge structures, even when noised measurement is considered.

Damage detection for truss bridge structures using correlation-based structural modal strain energy

This paper presents the feasibility of using structural modal strain energy as a parameter employed in correlation- based damage detection method for truss bridge structures. It is an extension of the damage detection method adopting multiple damage location assurance criterion. In this paper, the sensitivity of modal strain energy to damage obtained from the analytical model is incorporated into the correlation objective function. Firstly, the sensitivity matrix of modal strain energy to damage is conducted offline, and for an arbitrary damage case, the correlation coefficient (objective function) is calculated by multiplying the sensitivity matrix and damage vector. Then, a genetic algorithm is used to iteratively search the damage vector maximising the correlation between the corresponding modal strain energy change (hypothesised) and its counterpart in measurement. The proposed method is simulated and compared with the conventional methods, e.g. frequency-error method, coordinate modal assurance criterion and multiple damage location assurance criterion using mode shapes on a numerical truss bridge structure. The result demonstrates the modal strain energy correlation method is able to yield acceptable damage detection outcomes with less computing efforts, even in a noise contaminated condition.

Structural health monitoring : vibration-based damage detection and condition assessment of bridges

Structural health is a vital aspect of infrastructure sustainability. As a part of a vital infrastructure and transportation network, bridge structures must function safely at all times. However, due to heavier and faster moving vehicular loads and function adjustment, such as Busway accommodation, many bridges are now operating at an overload beyond their design capacity. Additionally, the huge renovation and replacement costs are a difficult burden for infrastructure owners. The structural health monitoring (SHM) systems proposed recently are incorporated with vibration-based damage detection techniques, statistical methods and signal processing techniques and have been regarded as efficient and economical ways to assess bridge condition and foresee probable costly failures. In this chapter, the recent developments in damage detection and condition assessment techniques based on vibration-based damage detection and statistical methods are reviewed. The vibration-based damage detection methods based on changes in natural frequencies, curvature or strain modes, modal strain energy, dynamic flexibility, artificial neural networks, before and after damage, and other signal processing methods such as Wavelet techniques, empirical mode decomposition and Hilbert spectrum methods are discussed in this chapter.

Pathogenicity of Plesiomonas shigelloides : interactions with eukaryotic host cells in vitro

Diarrhoea is one of the leading causes of morbidity and mortality in populations in developing countries and is a significant health issue throughout the world. Despite the frequency and the severity of the diarrhoeal disease, mechanisms of pathogenesis for many of the causative agents have been poorly characterised. Although implicated in a number of intestinal and extra-intestinal infections in humans, Plesiomonas shigelloides generally has been dismissed as an enteropathogen due to the lack of clearly demonstrated virulence-associated properties such as production of cytotoxins and enterotoxins or invasive abilities. However, evidence from a number of sources has indicated that this species may be the cause of a number of clinical infections. The work described in this thesis seeks to resolve this discrepancy by investigating the pathogenic potential of P. shigelloides using in vitro cell models. The focus of this research centres on how this organism interacts with human host cells in an experimental model. Very little is known about the pathogenic potential of P. shigel/oides and its mechanisms in human infections and disease. However, disease manifestations mimic those of other related microorganisms. Chapter 2 reviews microbial pathogenesis in general, with an emphasis on understanding the mechanisms resulting from infection with bacterial pathogens and the alterations in host cell biology. In addition, this review analyses the pathogenic status of a poorly-defined enteropathogen, P. shigelloides. Key stages of pathogenicity must occur in order for a bacterial pathogen to cause disease. Such stages include bacterial adherence to host tissue, bacterial entry into host tissues (usually required), multiplication within host tissues, evasion of host defence mechanisms and the causation of damage. In this study, these key strategies in infection and disease were sought to help assess the pathogenic potential of P. shigelloides (Chapter 3). Twelve isolates of P. shigelloides, obtained from clinical cases of gastroenteritis, were used to infect monolayers of human intestinal epithelial cells in vitro. Ultrastructural analysis demonstrated that P. shigelloides was able to adhere to the microvilli at the apical surface of the epithelial cells and also to the plasma membranes of both apical and basal surfaces. Furthermore, it was demonstrated that these isolates were able to enter intestinal epithelial cells. Internalised bacteria often were confined within vacuoles surrounded by single or multiple membranes. Observation of bacteria within membranebound vacuoles suggests that uptake of P. shigelloides into intestinal epithelial cells occurs via a process morphologically comparable to phagocytosis. Bacterial cells also were observed free in the host cell cytoplasm, indicating that P. shige/loides is able to escape from the surrounding vacuolar membrane and exist within the cytosol of the host. Plesiomonas shigelloides has not only been implicated in gastrointestinal infections, but also in a range of non-intestinal infections such as cholecystitis, proctitis, septicaemia and meningitis. The mechanisms by which P. shigelloides causes these infections are not understood. Previous research was unable to ascertain the pathogenic potential of P. shigel/oides using cells of non-intestinal origin (HEp-2 cells derived from a human larynx carcinoma and Hela cells derived from a cervical carcinoma). However, with the recent findings (from this study) that P. shigelloides can adhere to and enter intestinal cells, it was hypothesised, that P. shigel/oides would be able to enter Hela and HEp-2 cells. Six clinical isolates of P. shigelloides, which previously have been shown to be invasive to intestinally derived Caco-2 cells (Chapter 3) were used to study interactions with Hela and HEp-2 cells (Chapter 4). These isolates were shown to adhere to and enter both nonintestinal host cell lines. Plesiomonas shigelloides were observed within vacuoles surrounded by single and multiple membranes, as well as free in the host cell cytosol, similar to infection by P. shigelloides of Caco-2 cells. Comparisons of the number of bacteria adhered to and present intracellularly within Hela, HEp-2 and Caco-2 cells revealed a preference of P. shigelloides for Caco-2 cells. This study conclusively showed for the first time that P. shigelloides is able to enter HEp-2 and Hela cells, demonstrating the potential ability to cause an infection and/or disease of extra-intestinal sites in humans. Further high resolution ultrastructural analysis of the mechanisms involved in P. shigelloides adherence to intestinal epithelial cells (Chapter 5) revealed numerous prominent surface features which appeared to be involved in the binding of P. shige/loides to host cells. These surface structures varied in morphology from small bumps across the bacterial cell surface to much longer filaments. Evidence that flagella might play a role in bacterial adherence also was found. The hypothesis that filamentous appendages are morphologically expressed when in contact with host cells also was tested. Observations of bacteria free in the host cell cytosol suggests that P. shigelloides is able to lyse free from the initial vacuolar compartment. The vacuoles containing P. shigel/oides within host cells have not been characterised and the point at which P. shigelloides escapes from the surrounding vacuolar compartment has not been determined. A cytochemical detection assay for acid phosphatase, an enzymatic marker for lysosomes, was used to analyse the co-localisation of bacteria-containing vacuoles and acid phosphatase activity (Chapter 6). Acid phosphatase activity was not detected in these bacteria-containing vacuoles. However, the surface of many intracellular and extracellular bacteria demonstrated high levels of acid phosphatase activity, leading to the proposal of a new virulence factor for P. shigelloides. For many pathogens, the efficiency with which they adhere to and enter host cells is dependant upon the bacterial phase of growth. Such dependency reflects the timing of expression of particular virulence factors important for bacterial pathogenesis. In previous studies (Chapter 3 to Chapter 6), an overnight culture of P. shigelloides was used to investigate a number of interactions, however, it was unknown whether this allowed expression of bacterial factors to permit efficient P. shigelloides attachment and entry into human cells. In this study (Chapter 7), a number of clinical and environmental P. shigelloides isolates were investigated to determine whether adherence and entry into host cells in vitro was more efficient during exponential-phase or stationary-phase bacterial growth. An increase in the number of adherent and intracellular bacteria was demonstrated when bacteria were inoculated into host cell cultures in exponential phase cultures. This was demonstrated clearly for 3 out of 4 isolates examined. In addition, an increase in the morphological expression of filamentous appendages, a suggested virulence factor for P. shigel/oides, was observed for bacteria in exponential growth phase. These observations suggest that virulence determinants for P. shigel/oides may be more efficiently expressed when bacteria are in exponential growth phase. This study demonstrated also, for the first time, that environmental water isolates of P. shigelloides were able to adhere to and enter human intestinal cells in vitro. These isolates were seen to enter Caco-2 host cells through a process comparable to the clinical isolates examined. These findings support the hypothesis of a water transmission route for P. shigelloides infections. The results presented in this thesis contribute significantly to our understanding of the pathogenic mechanisms involved in P. shigelloides infections and disease. Several of the factors involved in P. shigelloides pathogenesis have homologues in other pathogens of the human intestine, namely Vibrio, Aeromonas, Salmonella, Shigella species and diarrhoeaassociated strains of Escherichia coli. This study emphasises the relevance of research into Plesiomonas as a means of furthering our understanding of bacterial virulence in general. As well it provides tantalising clues on normal and pathogenic host cell mechanisms.

Bearing damage analysis by calculation of capacitive coupling between inner and outer races of a ball bearing

Bearing damage in modern inverter-fed AC drive systems is more common than in motors working with 50 or 60 Hz power supply. Fast switching transients and common mode voltage generated by a PWM inverter cause unwanted shaft voltage and resultant bearing currents. Parasitic capacitive coupling creates a path to discharge current in rotors and bearings. In order to analyze bearing current discharges and their effect on bearing damage under different conditions, calculation of the capacitive coupling between the outer and inner races is needed. During motor operation, the distances between the balls and races may change the capacitance values. Due to changing of the thickness and spatial distribution of the lubricating grease, this capacitance does not have a constant value and is known to change with speed and load. Thus, the resultant electric field between the races and balls varies with motor speed. The lubricating grease in the ball bearing cannot withstand high voltages and a short circuit through the lubricated grease can occur. At low speeds, because of gravity, balls and shaft voltage may shift down and the system (ball positions and shaft) will be asymmetric. In this study, two different asymmetric cases (asymmetric ball position, asymmetric shaft position) are analyzed and the results are compared with the symmetric case. The objective of this paper is to calculate the capacitive coupling and electric fields between the outer and inner races and the balls at different motor speeds in symmetrical and asymmetrical shaft and balls positions. The analysis is carried out using finite element simulations to determine the conditions which will increase the probability of high rates of bearing failure due to current discharges through the balls and races.

Corneal confocal microscopy : a novel means to detect nerve fibre damage in idiopathic small fibre neuropathy

Patients with idiopathic small fibre neuropathy (ISFN) have been shown to have significant intraepidermal nerve fibre loss and an increased prevalence of impaired glucose tolerance (IGT). It has been suggested that the dysglycemia of IGT and additional metabolic risk factors may contribute to small nerve fibre damage in these patients. Twenty-five patients with ISFN and 12 aged-matched control subjects underwent a detailed evaluation of neuropathic symptoms, neurological deficits (Neuropathy deficit score (NDS); Nerve Conduction Studies (NCS); Quantitative Sensory Testing (QST) and Corneal Confocal Microscopy (CCM)) to quantify small nerve fibre pathology. Eight (32%) patients had IGT. Whilst all patients with ISFN had significant neuropathic symptoms, NDS, NCS and QST except for warm thresholds were normal. Corneal sensitivity was reduced and CCM demonstrated a significant reduction in corneal nerve fibre density (NFD) (Pb0.0001), nerve branch density (NBD) (Pb0.0001), nerve fibre length (NFL) (Pb0.0001) and an increase in nerve fibre tortuosity (NFT) (Pb0.0001). However these parameters did not differ between ISFN patients with and without IGT, nor did they correlate with BMI, lipids and blood pressure. Corneal confocal microscopy provides a sensitive non-invasive means to detect small nerve fibre damage in patients with ISFN and metabolic abnormalities do not relate to nerve damage.